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Human junctional epithelium as a pathway for inflammatory exudation
H E Schroeder1, K Rossinsky, M A Listgarten
1Department of Oral Structural Biology, University of Zurich, Switzerland.
Journal De Biologie Buccale
|September 1, 1989
Summary
Mild gingival inflammation causes enlarged intercellular spaces in junctional epithelium, exceeding normal cell turnover. Granulocytes actively migrate into the gingival sulcus, unlike lymphocytes.
Area of Science:
- Oral biology
- Histology
- Periodontology
Background:
- Gingival inflammation involves changes in the junctional and sulcular epithelium.
- Understanding these morphologic alterations is key to periodontitis research.
Purpose of the Study:
- To analyze morphologic changes in the dentogingival junction during mild gingival inflammation.
- To differentiate between inflammatory and artifactitious changes in epithelial intercellular spaces.
Main Methods:
- Utilized transmission electron microscopy (TEM) with photographic montages.
- Examined the dentogingival region, focusing on junctional and oral sulcular epithelium.
Main Results:
- Observed enlarged intercellular spaces in junctional epithelium, some containing granulocytes.
- Enlarged spaces showed intact intercellular bridges and preserved granulocytes, distinct from artifacts.
- Junctional epithelium turnover rate was insufficient to repair inflammatory-induced alterations.
- Granulocytes actively migrated through junctional epithelium into the gingival sulcus, while lymphocytes were passively carried.
Conclusions:
- Mild gingival inflammation significantly alters junctional epithelium morphology.
- Granulocyte migration is an active process in the inflamed gingival sulcus.
- Junctional epithelial cell turnover cannot fully compensate for inflammatory damage.